Background and aims Gitelman syndrome is a hereditary autosomal recessive abnormality of the kidney, that had presentation as hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. It is caused by mutation of SLC 12A3 gene encoding thiazide sensitive sodium-chloride co transporter. However, acquired Gitelman Syndrome can be found in SLE
Methods A 37 years old woman was admitted to hospital because of 7 days fever. She also had butterfly rash, hemolytic anaemia, and leucopenia. She was diagnosed as having SLE with hematologic and skin manifestation. Her sodium and potassium level were low. Her electrolyte imbalances were response well with supportive treatment. Ten days later, she had recurrent hypokalemia. Her haemoglobin level was decreased, and she was given packed red cell transfusion in her second admission.
Results One month later, she had neurologic manifestation, hemolytic anaemia, discoid rash, and low complement level. Her sodium, potassium, calcium, and magnesium levels were still low. High dose steroid and chloroquin were given. She was discharged from the hospital well, but had recurrent admission five days later due to spasm of the face and extremities, can’t open mouth, dyspnea, recurrent hyponatremia, hypokalemia, hypomagnesemia, and hypocalcemia. Her blood gas analysis showed metabolic alkalosis. She was diagnosed as having electrolity abnormality due to suspected acquired Gitelman syndrome.
Conclusions She was given pulse dose steroid, mycophenolate mofetil, and parenteral correction of electrolyte abnormality. She responsed well, and discharged from the hospital.
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